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The origin and evolution of viruses
- Origin and evolution of viruses: EscapedDNA/RNA sequences as evolutionaryaccelerators and natural biological weapons

In contrast to other microbes and multi-cellular organisms, the origin and evolution of viruses is mostly unknown. Our knowledge concerning their origin is lost in a sea of conjecture and speculations, hardly supported at all with precise scientific evidences. For example, viruses have never been detected as fossil particles, probably because they are too small and too fragile to succumb to fossilization processes. Even in fossilized biological materials such as plant leaves or insects in amber, preserved nucleic acid sequences of viruses have never been detected. Hence, evolutionists are limited in their ability to precisely reconstruct an evolutional history of viruses. However, in spite of all the difficulties in understanding their origin and evolution, several theories more or less successfully explain the basic observed facts [1–3].

Due to the fact that the genome of viruses underlies mutation and genetic recombination, viruses probably evolve according to a form of natural selection, very similar to that governing other living things. It seems that this simple fact may well provide enough support for scientific acceptability of several commonly discussed hypotheses on virus origin and evolution. Currently, there are three such hypotheses. The first hypothesis is the so-called theory of ‘‘regressive evolution’’, which proposes that viruses descend from free-living and more complex parasites. According to this theory, ancestral viruses developed a growing dependence on host-cell intracellular ‘‘machinery’’ through evolutionary time, while retaining the ability to auto-replicate, like mitochondria that have their own genetic information and replicate on their own [2–4]. The second hypothesis is the socalled theory of ‘‘cell origin’’, which assumes that viruses reflect their origin from cell DNA and/or messenger RNA, which acquired the ability to auto-replicate, create extracellular virions, exist and function independently. Finally, there is the theory of ‘‘independent’’ or ‘‘parallel’’ evolution of viruses and other organisms, which assumes that viruses appeared at the same time as the most primitive organisms [1,3,4].

Whatever the advantages and disadvantages of each theory are, the ability of every cell (excluding cells without a nucleus, e.g., the erythrocytes of mammals) to release DNA/RNA sequences or de novo created viruses is unique and amazing. At the same time, the cell’s ability to release DNA/ RNA sequences shows a high level of evolutionary conservation. These facts might be well enough motifs for identification of positive selective pressure that could be linked with this genome ability, as well as a highly important thesis for better understanding of origin and evolution of viruses, and even life as we know it [3–5]. Several factors of positive selective pressure could play important role in development and evolutionary ‘‘symbiotic’’ linking (conservation) of genome and its ‘‘instability’’, which is probably responsible for cell ability to emit de novo created viruses: (i) the possibility of horizontal and vertical dissemination of gene blocks, and their incorporation into the cell genome of new hosts; (ii) the possibility of acceleration of evolutionary processes, which could result in rapid diversification of species and sometimes quicker and better adapting to environmental conditions; (iii) the possibility that de novo created viruses can act as natural biological weapons against predator and/or concurrent species.

There are a number of complex molecular life forms that blur the boundaries between cells and viruses. Also, there are pieces of self-replicating genetic material found in bacteria, e.g., episomes, which evolve independently of their hosts, and can even move from one host to another – but carry genetic information that may be toxic or beneficial, even essential, to their host. In the case of the beneficial role of episomes, many bacteria would be unable to reproduce at all without them. Episomes are, in many ways, quite similar to viruses – except that they only reproduce themselves when their hosts do, whereas viruses reproduce themselves hundreds of times, causing disease. According to this way of thinking, viruses probably co-evolve with their hosts, like any ‘‘good parasite’’. There appears to be quite a lot of justification for this idea, especially from studies of viruses such as papilloma viruses, endogenous retrovirus- like sequences in animal genomes, and herpes viruses. For example, the divergences of primates and of birds related to chickens have been traced by comparing the types and sequences of retroviral-derived sequences in their genomes. It has also been repeatedly shown that the closest relatives of human papillomavirus types infecting particular tissue types (e.g., cutaneous wart types, genital mucosal types) are those viruses infecting similar tissue types in other primates, indicating that these tissue preferences were well established before the divergence of humanoid apes from the primate line [1,3,4].

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